Fig. 4. Effects of ACO on the kinetics of peak I_Na in guinea pig ventricular myocytes.

a The time courses of the peak I_Na in the presence of ACO or TTX. b Representative traces of peak I_Na recorded in the presence of ACO or TTX. The inset shows a schematic of the voltage-clamp protocol. c Summarized data of the effects of the percentage increase in ACO on the peak I_Na (five cells from three guinea pig hearts in each group). d The concentration-response curves of the effects of ACO on peak I_Na. The concentration-response relationships were fitted by a logistic function. e Summarized data of the I–V relationship of peak I_Na after 100 μM ACO treatment. f Typical traces of steady-state activation of peak I_Na before and after ACO treatment. The inset shows a schematic of the protocol. g Summarized data of steady-state activation of peak I_Na. h Representative peak I_Na traces of steady-state inactivation before and after ACO treatment. The inset shows a schematic of the voltage -clamp protocol. i Summarized data of steady-state inactivation curves of peak I_Na. j Representative peak I_Na recovery traces from inactivation in response to voltage commands consisting of two −20 mV depolarization pulses (P1 and P2) from a holding potential of −90 mV, separated by a 1–20-ms or a 20–500-ms variable interval (P1–P2) at −90 mV before and after ACO treatment. The inset shows a schematic of the voltage-clamp protocol. k Normalized peak I_Na recovery (P2/P1) vs. interpulse interval at −90 mV. There were seven cells from three guinea pig hearts in each group. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001 vs. control group; ^#P < 0.05, vs. 0.3 μM ACO group.